Afferent arteriole (Af-Art) resistance is modulated by 2 intrinsic nephron feedbacks: 1) vasoconstrictor tubuloglomerular feedback (TGF), which is mediated by NKCC2 in the macula densa and blocked by furosemide; and 2) vasodilator connecting tubule glomerular feedback (CTGF), which is mediated by ENaC in the connecting tubule and blocked by benzamil. High salt intake reduces the Af-Art vasoconstrictor ability in Dahl salt-sensitive rats (Dahl SS). Previously, we measured CTGF indirectly using the differences between the TGF responses with and without CTGF inhibition. We recently developed a method to measure CTGF more directly by simultaneously inhibiting NKCC2 and the Na/H exchanger (NHE). We hypothesize that during the simultaneous inhibition of NKCC2 and NHE in vivo, CTGF causes Af-Art dilatation, as reflected by an increase in stop-flow pressure (PSF) in Dahl SS that is enhanced with a high salt intake. In the presence of furosemide alone, increasing nephron perfusion did not change the PSF in either Dahl salt-resistant rats (Dahl SR) or in Dahl SS. When furosemide and the NHE inhibitor dimethylamiloride were perfused simultaneously, the increased tubular flow caused Af-Art dilatation, as demonstrated by increased PSF. This increase was greater in Dahl SS (4.5±0.4 mmHg) than in Dahl SR (2.5±0.3 mmHg; P < 0.01). CTGF causes this vasodilation since benzamil completely blocked this effect. However, a high salt intake did not augment Af-Art dilatation. We conclude that during the simultaneous inhibition of NKCC2 and NHE in the nephron, CTGF induces Af-Art dilatation, and a high salt intake failed to enhance this effect.